Offspring receive differential early somatosensory stimulation through parenting and other processes, such as neonatal exposure to novelty. This early somatosensory stimulation is known to have long-term effects on the development of stress reactivity and social behavior. These early differences in somatosensory stimulation may also contribute both to normal and pathological development of sensory function. A wide variety of developmental disorders share many characteristics including a developmental timeline and dysregulation of both social behavior and somatosensory function. The aim of the current proposal is to examine the effects of early environment, in particular the effects of early somatosensory stimulation on later social and sensory behavior, and on the functional organization and size of the primary somatosensory cortex (S1) in a rodent model, the prairie vole (Microtus ochrogaster). First, normal development will be studied in offspring from parents which demonstrate extremes of natural individual variation in somatosensory stimulation. We will then examine offspring from a handling model known to produce deficits in social behavior, and which has been shown to exert its effects through differential early somatosensory stimulation of young. Following weaning, anxiety, social behavior, and sensorimotor gating in the offspring will be examined, as well as the functional organization and size of S1, and its thalamocortical and cortico-cortical connections. Finally, all of these variables will be correlated: early somatosensory stimulation received from parents, later social, anxiety, and sensory behavior, and neuroanatomical organization of S1. PUBLIC HEALTH RELEVANCE: Many developmental disorders exhibit changes in both social behavior and sensory function. This proposal will investigate how environmental factors in early life can lead to changes in behavior and in the function of the somatosensory cortex.